Ryanodine, a diterpenoid poison derived from Ryania speciosa, acts as a modulator of the ryanodinereceptor, which is permeable to cells. Depending on its concentration, ryanodine can either stimulate or inhibit Ca2+ release mediated by these receptors.
Cyclic ADP-ribose (cADPR) is an effective calcium mobilization second messenger, which is synthesized from NAD + by ADP-ribosyl cyclase. Cyclic ADP-ribose mainly increases cytosolic calcium through Ryanodinereceptor-mediated endoplasmic reticulum release
Cyclic ADP-ribose ammonium (cADPR ammonium) is a powerful calcium mobilization second messenger synthesized from NAD+ by an ADP-ribosyl cyclase. It primarily raises cytosolic calcium levels through Ryanodinereceptor-mediated release from the endoplasmic reticulum, while also facilitating extracellular influx through the opening of TRPM2 channels [1][2][3].
Azumolene sodium dihydrate is a muscle relaxant that inhibits the release of calcium from skeletal muscle sarcoplasmic reticulum. Azumolene inhibits a component of store-operated calcium entry coupled to the skeletal muscle ryanodinereceptor.
Azumolene sodium anhydrous is a muscle relaxant that inhibits the release of calcium from skeletal muscle sarcoplasmic reticulum. Azumolene inhibits a component of store-operated calcium entry coupled to the skeletal muscle ryanodinereceptor. Azumolene, an equipotent dantrolene analog, inhibits a component of SOCE coupled to activation of RyR1 by caffeine and ryanodine, whereas the SOCE component induced by thapsigargin is not affected.
ent-(+)-verticilide is an effective and specific inhibitor of cardiac ryanodinereceptor (RyR2) calcium release channels, demonstrating antiarrhythmic properties. It suppresses RyR2-mediated diastolic Ca2+ leak and shows greater potency and a unique action mechanism compared to Dantrolene and Tetracaine. ent-(+)-verticilide serves as a valuable tool for exploring the therapeutic potential of addressing RyR2 hyperactivity in cardiac and neurological conditions [1].